Abstract
In December 2019, rising pneumonia cases caused by a novel β-coronavirus (SARS-CoV-2) occurred in Wuhan, China, which has rapidly spread worldwide, causing thousands of deaths. The WHO declared the SARS-CoV-2 outbreak as a public health emergency of international concern, since then several scientists are dedicated to its study. It has been observed that many human viruses have codon usage biases that match highly expressed proteins in the tissues they infect and depend on the host cell machinery for the replication and co-evolution. In this work, we analysed 91 molecular features and codon usage patterns for 339 viral genes and 463 human genes that consisted of 677,873 codon positions. Hereby, we selected the highly expressed genes from human lung tissue to perform computational studies that permit to compare their molecular features with those of SARS, SARS-CoV-2 and MERS genes. The integrated analysis of all the features revealed that certain viral genes and overexpressed human genes have similar codon usage patterns. The main pattern was the A/T bias that together with other features could propitiate the viral infection, enhanced by a host dependant specialization of the translation machinery of only some of the overexpressed genes. The envelope protein E, the membrane glycoprotein M and ORF7 could be further benefited. This could be the key for a facilitated translation and viral replication conducting to different comorbidities depending on the genetic variability of population due to the host translation machinery. This is the first codon usage approach that reveals which human genes could be potentially deregulated due to the codon usage similarities between the host and the viral genes when the virus is already inside the human cells of the lung tissues. Our work leaded to the identification of additional highly expressed human genes which are not the usual suspects but might play a role in the viral infection and settle the basis for further research in the field of human genetics associated with new viral infections. To identify the genes that could be deregulated under a viral infection is important to predict the collateral effects and determine which individuals would be more susceptible based on their genetic features and comorbidities associated.
Highlights
Since its initial outbreak at Huanan Seafood Wholesale Market in Wuhan, China, in late 2019, COVID-19 has affected more than 4 million people and caused more than 300 thousand deaths all around the world
In order to contribute to the insight of the virus and its molecular features, here we provide a thorough and comprehensive analysis of codon usage and the molecular features of the viral genes and highly expressed genes in human lung tissue that allowed us to find particular similarities between specific viral and human genes that could help to understand the viability of the virus as well as the susceptibility of the humans to the viral infection based on the molecular features of their genes
A phylogenetic tree was constructed using the whole genome sequences of severe acute respiratory syndrome (SARS)-CoV-2 reported in humans from Spain, USA, Italy, South America, China, Korea, Japan, Australia, the refseq genomes of Middle East respiratory syndrome (MERS) and SARS and the viruses genomes that were isolated from bats, pangolins, civets, hedgehogs, Bos taurus, and canids (Supplementary Information 1)
Summary
Since its initial outbreak at Huanan Seafood Wholesale Market in Wuhan, China, in late 2019, COVID-19 has affected more than 4 million people and caused more than 300 thousand deaths all around the world. Thereafter, scientists are focused on studying the biology and dissemination of COVID-19 to control the transmission and design proper diagnostic tools and treatments, and they are racing to design a vaccine that could prevent the infection caused by the coronavirus SARS-CoV-2 This virus belongs to the Betacoronavirus (β-coronavirus) of the Coronaviridae family, which is composed of three more genera: Alphacoronavirus (αCoV), Gammacoronavirus (γCoV), and Deltacoronavirus (δCoV)[1]. Our work revealed molecular and evolutionary aspects of the human coronaviruses SARSCoV-2, SARS and MERS that helps to determine whether the level of similarity of the codon usage and the molecular features between the highly expressed genes in human lung tissue and the genes of the coronaviruses are responsible for the codons selection in the viruses and whether these could propitiate viral infections. Since the molecules of the translation machinery of the overexpressed genes should be in the proper abundance to fit the needs of the protein translation of the host, the virus can take advantage from this to synthetise their own particles to the detriment of the normal function of the host cells
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